Disseminated toxoplasmosis in black-footed penguins (Spheniscus demersus).

Three 1- to 3-mo-old black-footed penguins (Spheniscus Demersus) died within 24 hr of showing central nervous signs such as ataxia. The birds were housed in a baby penguin crèche. At necropsy, peritonitis, pneumonia, hepatomegaly, splenomegaly, and renomegaly were evident. Histologically, the liver, lung, brain, and small intestine contained numerous tachyzoites and a few cysts of Toxoplasma. Immunohistochemistry identified the protozoal parasites as Toxoplasma gondii. Ultrastructurally, this was confirmed by the presence of many tachyzoites of T. gondii in the liver and lungs.

Salmonella serovar specific upregulation of porcine defensins 1 and 2 in a jejunal epithelial cell line.

Defensins are important antimicrobial effector peptides of the innate immune system, which provides protection against bacterial infections in the intestine. Salmonella Choleraesuis and Salmonella Typhimurium are the most commonly isolated serovars in pig, but disease outcome is dependent on the Salmonella serovar. These infections are a serious problem for the swine industry and are also posing a major threat to public health because of Salmonella-related food-borne illnesses in human. To understand the innate immune response of pigs upon Salmonella infections, we studied the effect of these Salmonella serovars on defensin gene expression in the porcine ileal epithelial cell line IPEC-J2. With the use of scanning electron microscopy, we first visualized the surface characteristics of this cell line, and captured the invasion of Salmonella into the epithelial cell. Gene expression levels of porcine beta-defensin 1 and 2 were both induced upon S. Typhimurium infection but S. Choleraesuis had no effect. Invasion, adhesion and defensin susceptibility of both serovars were similar, which could not explain the observed difference in host response to these Salmonellae. In addition, induction of defensins was dependent on viability of S. Typhimurium, since Salmonella cell- or secreted components had no effect on defensin gene expression. These results provide further insight into the porcine innate immune response towards Salmonella infections, and could partially explain the different epidemiology of Salmonella infections in pig.

Interaction of Arcobacter spp. with human and porcine intestinal epithelial cells.

Little is known about the pathogenic mechanisms or potential virulence factors of Arcobacter spp. The aim of the study described here was to obtain more insights in the pathogenicity mechanisms of Arcobacter spp. by testing their ability to adhere to, invade and induce interleukin-8 expression in human Caco-2 and porcine IPI-2I cell lines. Eight Arcobacter strains were tested. Four strains were obtained from a culture collection, and represent the four Arcobacter spp. known to be associated with animals and humans. The other four strains were field isolates from the amniotic fluid of sows and from newborn piglets. All eight Arcobacter strains were able to adhere to both cell lines, and induced interleukin-8 production as early as 2 h after a 1h incubation period. This production was still increased 6 h postinfection. Differences in the cell association of the eight strains were obvious, with A. cibarius showing the highest adhesion ability. Invasion of intestinal epithelial cells was only observed for A. cryaerophilus strains. No correlation between invasiveness or strong adhesion of the tested strains and the level of interleukin-8 induction was observed.

Morphological characterisation of portal myofibroblasts and hepatic stellate cells in the normal dog liver.

BACKGROUND: Hepatic fibrosis is a common outcome of hepatic injury in both man and dog. Activated fibroblasts which develop myofibroblastic characteristics play an essential role in hepatic fibrogenesis, and are comprised of three subpopulations: 1) portal or septal myofibroblasts, 2) interface myofibroblasts and 3) the perisinusoidally located hepatic stellate cells (HSC). The present study was performed to investigate the immunohistochemical characteristics of canine portal myofibroblasts (MF) and HSC in the normal unaffected liver as a basis for further studies on fibrogenesis in canine liver disease. RESULTS: In the formalin-fixed and paraffin embedded normal canine liver vimentin showed staining of hepatic fibroblasts, probably including MF in portal areas and around hepatic veins; however, HSC were in general negative. Desmin proved to react with both portal MF and HSC. A unique feature of these HSC was the positive immunostaining for alpha-smooth muscle actin (alpha-SMA) and muscle-specific actin clone HHF35 (HHF35), also portal MF stained positive with these antibodies. Synaptophysin and glial fibrillary acidic protein (GFAP) were consistently negative in the normal canine liver. In a frozen chronic hepatitis case (with expected activated hepatic MF and HSC), HSC were negative to synaptophysin, GFAP and NCAM. Transmission electron microscopy (TEM) immunogold labelling for alpha-SMA and HHF35 recognized the positive cells as HSC situated in the space of Disse. CONCLUSION: In the normal formalin-fixed and paraffin embedded canine liver hepatic portal MF and HSC can be identified by alpha-SMA, HHF35 and to a lesser extent desmin immunostaining. These antibodies can thus be used in further studies on hepatic fibrosis. Synaptophysin, GFAP and NCAM do not seem suitable for marking of canine HSC. The positivity of HSC for alpha-SMA and HHF35 in the normal canine liver may eventually reflect a more active regulation of hepatic sinusoidal flow by these HSC compared to other species.